...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of Cellular Physiology >Rab11b and its effector Rip11 regulate the acidosis-induced traffic of V-ATPase in salivary ducts.
【24h】

Rab11b and its effector Rip11 regulate the acidosis-induced traffic of V-ATPase in salivary ducts.

机译：Rab11b及其效应Rip11调节acidosis-induced交通V-ATPase的唾液导管。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Redistribution of acid-base transporters is a crucial regulatory mechanism for many types of cells to cope with extracellular pH changes. In epithelial cells, however, translocation of acid-base transporters ultimately leads to changes in vectorial transport of H+ and HCO3-. We have previously shown that the bicarbonate-secreting epithelium of salivary ducts responds to changes of systemic acid-base balance by adaptive redistribution of H+ and HCO3- transporters, thereby influencing the ionic composition and buffering capacity of saliva. However, the specific proteins involved in regulated vesicular traffic of acid-base transporters are largely unknown. In the present study we have investigated the impact of Rab11 family members on the acidosis-induced trafficking of the vacuolar-type H+-ATPase (V-ATPase) in salivary duct cells in vitro using the human submandibular cell line of ductal origin HSG as an experimental model. The results show that Rab11b is expressed in salivary ducts and exhibits a significantly higher co-localization with V-ATPase than Rab11a and Rab25. We also show that Rab11 but not Rab25 interacts with the epsilon subunit of V-ATPase. Extracellular acidosis up-regulates Rab11b expression and protein abundance in HSG cells and causes translocation of the V-ATPase from intracellular pools toward the plasma membrane. Loss-of-function experiments using specific siRNA either against Rab11b or against its effector Rip11 prevent acidosis-induced V-ATPase translocation. These data introduce Rab11b as a crucial regulator and Rip11 as mediator of acidosis-induced V-ATPase traffic in duct cells of submandibular gland.
机译：酸碱转运蛋白是一种再分配对于许多类型的至关重要的监管机制细胞应对细胞外的pH值变化。上皮细胞,然而,易位酸碱转运蛋白最终导致的变化矢量传输H +和HCO3 -。我们以前曾证实bicarbonate-secreting上皮的唾导管系统性酸碱的响应变化H +的自适应分配和平衡HCO3 -转运蛋白,从而影响离子成分和唾液的缓冲能力。然而,特定的蛋白质参与监管水泡酸碱的交通转运蛋白在很大程度上是未知的。研究中我们调查了Rab11的影响家庭成员在acidosis-induced贩卖vacuolar-type H + atp酶(V-ATPase)唾管细胞体外使用人类颌下导管的细胞系起源HSG集团作为实验模型。表明Rab11b唾液腺中表达和展品更高与比Rab11a V-ATPase co-localizationRab25。与V-ATPase的ε亚基。细胞外酸中毒让Rab11bHSG细胞和表达和蛋白质丰富导致V-ATPase的易位细胞内池向质膜。使用特定的核功能丧失的实验针对Rab11b或对其效应Rip11防止acidosis-induced V-ATPase易位。至关重要的监管机构和Rip11中介acidosis-induced V-ATPase交通管细胞颌下腺。

著录项

相似文献

  • 外文文献
  • 中文文献
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号